Journal of cellular signaling最新文献_第8页

Cancer-associated Molecular Abnormalities in Human NK cells 人类NK细胞中与癌症相关的分子异常

Journal of cellular signaling Pub Date : 2021-06-30 DOI: 10.33696/signaling.2.039

G. Zakiryanova, M. Shurin

引用次数: 1

Possible Therapeutic Use of Natural Compounds Against COVID-19 天然化合物抗COVID-19的可能治疗用途

Journal of cellular signaling Pub Date : 2021-02-18 DOI: 10.33696/SIGNALING.2.036

Nabab Khan, Xuesong Chen, J. Geiger

引用次数: 20

S1P Generation by Sphingosine Kinase-2 in Recruited Macrophages Resolves Lung Inflammation by Blocking STING Signaling in Alveolar Macrophages 鞘氨醇激酶-2在募集的巨噬细胞中产生S1P，通过阻断肺泡巨噬细胞的STING信号解决肺部炎症

Journal of cellular signaling Pub Date : 2021-02-02 DOI: 10.33696/SIGNALING.2.034

J. Joshi, Bhagwati Joshi, Ian Rochford, D. Mehta

引用次数: 3

FOXP1 Interacts with MyoD to Repress its Transcription and Myoblast Conversion FOXP1与MyoD相互作用抑制其转录和成肌细胞转化

Journal of cellular signaling Pub Date : 2021-01-11 DOI: 10.33696/SIGNALING.2.032

W. Wright, Chuan Li, Chang-xue Zheng, Haley O. Tucker

{"title":"FOXP1 Interacts with MyoD to Repress its Transcription and Myoblast Conversion","authors":"W. Wright, Chuan Li, Chang-xue Zheng, Haley O. Tucker","doi":"10.33696/SIGNALING.2.032","DOIUrl":"https://doi.org/10.33696/SIGNALING.2.032","url":null,"abstract":"Forkhead transcription factors (TFs) often dimerize outside their extensive family, whereas bHLH transcription factors typically dimerize with E12/E47. Based on structural similarities, we predicted that a member of the former, Forkhead Box P1 (FOXP1), might heterodimerize with a member of the latter, MYOD1 (MyoD). Data shown here support this hypothesis and further demonstrate the specificity of this forkhead/myogenic interaction among other myogenic regulatory factors. We found that FOXP1-MyoD heterodimerization compromises the ability of MyoD to bind to E-boxes and to transactivate E box- containing promoters. We observed that FOXP1 is required for the full ability of MyoD to convert fibroblasts into myotubules. We provide a model in which FOXP1 displaces ID and E12/E47 to repress MyoD during the proliferative phase of myoblast differentiation. These data identify FOXP1 as a hitherto unsuspected transcriptional repressor of MyoD. We suggest that isolation of paired E-box and forkhead sites within 1 turn helical spacings provides potential for cooperative interactions among heretofore distinct classes of transcription factors.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"1 1","pages":"9 - 26"},"PeriodicalIF":0.0,"publicationDate":"2021-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82456910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

FOXP1 Interacts with MyoD to Repress its Transcription and Myoblast Conversion. FOXP1与MyoD相互作用抑制其转录和成肌细胞转化。

Journal of cellular signaling Pub Date : 2021-01-01

Woodring E Wright, Chuan Li, Chang-Xue Zheng, Haley O Tucker

{"title":"FOXP1 Interacts with MyoD to Repress its Transcription and Myoblast Conversion.","authors":"Woodring E Wright, Chuan Li, Chang-Xue Zheng, Haley O Tucker","doi":"","DOIUrl":"","url":null,"abstract":"Forkhead transcription factors (TFs) often dimerize outside their extensive family, whereas bHLH transcription factors typically dimerize with E12/E47. Based on structural similarities, we predicted that a member of the former, Forkhead Box P1 (FOXP1), might heterodimerize with a member of the latter, MYOD1 (MyoD). Data shown here support this hypothesis and further demonstrate the specificity of this forkhead/myogenic interaction among other myogenic regulatory factors. We found that FOXP1-MyoD heterodimerization compromises the ability of MyoD to bind to E-boxes and to transactivate E box- containing promoters. We observed that FOXP1 is required for the full ability of MyoD to convert fibroblasts into myotubules. We provide a model in which FOXP1 displaces ID and E12/E47 to repress MyoD during the proliferative phase of myoblast differentiation. These data identify FOXP1 as a hitherto unsuspected transcriptional repressor of MyoD. We suggest that isolation of paired E-box and forkhead sites within 1 turn helical spacings provides potential for cooperative interactions among heretofore distinct classes of transcription factors.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"2 1","pages":"9-26"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7861563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25343838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Plasminogen Activator Inhibitor-1 and Oncogenesis in the Liver Disease. 纤溶酶原激活物抑制剂-1与肝病的肿瘤发生。

Journal of cellular signaling Pub Date : 2021-01-01 DOI: 10.33696/signaling.2.054

Da-Eun Nam, Hae Chang Seong, Young S Hahn

{"title":"Plasminogen Activator Inhibitor-1 and Oncogenesis in the Liver Disease.","authors":"Da-Eun Nam, Hae Chang Seong, Young S Hahn","doi":"10.33696/signaling.2.054","DOIUrl":"https://doi.org/10.33696/signaling.2.054","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a significant cause of cancer mortality worldwide. Chronic hepatic inflammation and fibrosis play a critical role in the development of HCC. Liver fibrosis develops as a result of response to injury such that a persistent and excessive wound healing response induces extracellular matrix (ECM) deposition leading to HCC. PAI-1 is a fibrinolysis inhibitor involved in regulating protein degradation and homeostasis while assisting wound healing. PAI-1 presents increased levels in various diseases such as fibrosis, cancer, obesity and metabolic syndrome. Moreover, PAI-1 has been extensively studied for developing potential therapies against fibrosis. In the present review, we summarize how PAI-1 affects oncogenesis during liver disease progression based on the recently published literatures. Although there are controversies regarding the role of PAI-1 and approaches to treatment, this review suggests that proper manipulation of PAI-1 activity could provide a novel therapeutic option on the development of chronic liver disease via modulation of cancer stem-like cells (CSCs) differentiation.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"2 3","pages":"221-227"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8525887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39535965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

NH₂-Terminal Cleavage of Cardiac Troponin I Signals Adaptive Response to Cardiac Stressors. 心肌肌钙蛋白I的nh2末端切割信号对心脏应激源的适应性反应。

Journal of cellular signaling Pub Date : 2021-01-01

Chad M Warren, Monika Halas, Han-Zhong Feng, Beata M Wolska, Jian-Ping Jin, R John Solaro

{"title":"NH2-Terminal Cleavage of Cardiac Troponin I Signals Adaptive Response to Cardiac Stressors.","authors":"Chad M Warren, Monika Halas, Han-Zhong Feng, Beata M Wolska, Jian-Ping Jin, R John Solaro","doi":"","DOIUrl":"","url":null,"abstract":"Cardiac sarcomeres express a variant of troponin I (cTnI) that contains a unique N-terminal extension of ~30 amino acids with regulatory phosphorylation sites. The extension is important in the control of myofilament response to Ca2+, which contributes to the neuro-humoral regulation of the dynamics of cardiac contraction and relaxation. Hearts of various species including humans express a stress-induced truncated variant of cardiac troponin I (cTnI-ND) missing the first ~30 amino acids and functionally mimicking the phosphorylated state of cTnI. Studies have demonstrated that upregulation of cTnI-ND potentially represents a homeostatic mechanism as well as an adaptive response in pathophysiology including ischemia/reperfusion injury, beta adrenergic maladaptive activation, and aging. We present evidence showing that cTnI-ND can modify the trigger for hypertrophic cardiomyopathy (HCM) by reducing the Ca2+ sensitivity of myofilaments from hearts with an E180G mutation in α-tropomyosin. Induction of this truncation may represent a therapeutic approach to modifying Ca2+-responses in hearts with hypercontractility or heat failure with preserved ejection fraction.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"2 3","pages":"162-171"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/26/b5/nihms-1735512.PMC8444995.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39453025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neoadjuvant Therapy (NAT) in Localized Pancreatic Cancer: Should We Do It and What Should We Do? 新辅助治疗(NAT)在局部胰腺癌中的应用:我们应该做什么?

Journal of cellular signaling Pub Date : 2021-01-01 DOI: 10.33696/signaling.2.037

Shreya Prasad Goyal, Morana Vojnic, Jung-In Yang, Jyothi Jose, Elliot Newman, M Wasif Saif

{"title":"Neoadjuvant Therapy (NAT) in Localized Pancreatic Cancer: Should We Do It and What Should We Do?","authors":"Shreya Prasad Goyal, Morana Vojnic, Jung-In Yang, Jyothi Jose, Elliot Newman, M Wasif Saif","doi":"10.33696/signaling.2.037","DOIUrl":"https://doi.org/10.33696/signaling.2.037","url":null,"abstract":"In 2019, approximately 56,770 new cases of pancreatic cancer were diagnosed in the United States, resulting in an estimated 45,750 deaths. Pancreatic cancer is one of the leading causes of cancer-related death, with a five-year survival rate of 9% [1]. Based on the eighth edition of the American Joint Committee on Cancer (AJCC) staging system for pancreatic adenocarcinoma, multi-center analyses have validated that poorer prognosis is associated with node-positive disease (N1 and N2) [2,3]. Specifically, five-year survival rates were significantly lower with the increasing N stage: 35.6% in N0, 20.8% in N1, and 10.9% in N2, reflecting relatively better survival in organ confined pancreatic cancer, compared to node positive disease [3]. To date, the most effective treatment for pancreatic cancer is known to be surgical resection, partly due to the intrinsic resistance of pancreatic cancer cells to systemic therapy or radiotherapy. Unfortunately, only 15–20% of patients are candidates for surgical resection as most patients are diagnosed with locally advanced or metastatic disease, due to a lack of effective pancreatic cancer screening methods. However, the prognosis of pancreatic cancer is still grim even in those with resectable disease.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"2 1","pages":"80-84"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8336067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39280746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting Cullin-RING E3 Ubiquitin Ligase 4 by Small Molecule Modulators. 小分子调节剂靶向Cullin-RING E3泛素连接酶4

Journal of cellular signaling Pub Date : 2021-01-01 DOI: 10.33696/Signaling.2.051

Kenneth Wu, Benjamin D Hopkins, Roberto Sanchez, Robert J DeVita, Zhen-Qiang Pan

引用次数: 0

APE1/Ref-1 as a Novel Target for Retinal Diseases. 作为视网膜疾病新靶点的 APE1/Ref-1

Journal of cellular signaling Pub Date : 2021-01-01 DOI: 10.33696/Signaling.2.044

Curtis Heisel, Jonah Yousif, Mahmut Mijiti, Kostas Charizanis, Mitchel Brigell, Timothy W Corson, Mark R Kelley

{"title":"APE1/Ref-1 as a Novel Target for Retinal Diseases.","authors":"Curtis Heisel, Jonah Yousif, Mahmut Mijiti, Kostas Charizanis, Mitchel Brigell, Timothy W Corson, Mark R Kelley","doi":"10.33696/Signaling.2.044","DOIUrl":"10.33696/Signaling.2.044","url":null,"abstract":"APE1/Ref-1 (also called Ref-1) has been extensively studied for its role in DNA repair and reduction-oxidation (redox) signaling. The review titled: \"The multifunctional APE1 DNA repair-redox signaling protein as a drug target in human disease\" by Caston et. al. summarizes the molecular functions of Ref-1 and the role it plays in a number of diseases, with a specific focus on various types of cancer [1]. Previous studies have demonstrated that Ref-1 plays a critical role in regulating specific transcription factors (TFs) involved in a number of pathways, not only in cancer, but other disease indications as well. Disease indications of particular therapeutic interest include retinal vascular diseases such as diabetic retinopathy (DR), diabetic macular edema (DME), and neovascular age-related macular degeneration (nvAMD). While Ref-1 controls a number of TFs that are under redox regulation, three have been found to directly link cancer studies to retinal diseases; HIF-1α, NF-κB and STAT3. HIF-1α controls the expression of VEGF for angiogenesis while NF-κB and STAT3 regulate a number of known cytokines and factors involved in inflammation. These pathways are highly implicated and validated as major players in DR, DME and AMD. Therefore, findings in cancer studies for Ref-1 and its inhibition may be translated to these ocular diseases. This report discusses the path from cancer to the potential treatment of retinal disease, the Ref-1 redox signaling function as a possible target, and the current small molecules which have been identified to block this activity. One molecule, APX3330, is in clinical trials, while the others are in preclinical development. Inhibition of Ref-1 and its effects on inflammation and angiogenesis makes it a potential new therapeutic target for the treatment of retinal vascular diseases. This commentary summarizes the retinal-relevant research that built on the results summarized in the review by Caston et. al. [1].","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"2 2","pages":"133-138"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8315574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39254413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0